The broad goal of this research is to provide a window into those aspects of the cognitive architecture of the lexical processing system that are impaired and those that are spared in aphasia and to examine the neural systems underlying such processing. Specific aims are to examine lexical processing and the effects of competition on mapping from sound to meaning in auditory word recognition and on mapping from meaning to sound in spoken word production to test three hypotheses. Hypothesis 1: Access to lexical form recruits parietal areas including the supramarginal gyrus (SMG), whereas access to lexical meaning recruits frontal areas including the inferior frontal gyrus (IFG). It is hypothesized that under conditions of lexical competition Conduction aphasics with parietal damage including the SMG will exhibit deficits when accessing phonological form under conditions of lexical competition and Broca's aphasics with frontal lesions including the IFG will exhibit deficits when accessing lexical meaning under conditions of lexical competition. Hypothesis 2: Aphasic patients have normal interactive processes. This hypothesis will be tested in two ways. First, based on normal results in spoken word production showing the influence of phonological lexical competition on processes downstream from it, i.e. on acoustic phonetic output, it is hypothesized that both Wernicke's aphasics with lesions including the superior temporal gyrus (STG) and Conduction aphasics with lesions including the SMG who show impairments in accessing lexical form under conditions of lexical competition will show smaller or no influence of lexical competition on their acoustic-phonetic output. In contrast, Broca's aphasics with IFG lesions who show normal patterns of performance under such conditions will show lexical competition effects on their acoustic-phonetic output. Second, it is hypothesized that information from higher-level sources including lexical-semantics and sentence context will override lexical deficits that emerge under conditions of phonological competition. Hypothesis 3: Lexical deficits in aphasia are not independently affected in auditory word recognition and spoken word production, implicating a central deficit. Thus, Conduction aphasic patients with SMG lesions who show deficits in auditory word recognition under conditions of phonological lexical competition should show concomitant impairments in spoken word production, and Broca's aphasics with lesions involving the IFG who show normal patterns of performance in auditory word recognition under conditions of phonological lexical competition should show normal patterns of performance in spoken word production. To test these hypotheses, we will use a variety of experimental paradigms including eye-tracking, same-different judgment, lexical decision, semantic priming, and word reading and picture naming followed by acoustic analysis of the spoken output. Relevance: Understanding the basis of these impairments is one step towards to development of appropriate rehabilitation strategies.